complete explanation with amicable pictures regarding CNS stimulants and cognitive enhancers.useful for both UG and PG students.references from different books and authors
ANTIDEPRESSANTS: All you need to know...by RxVichu! :)RxVichuZ
This is my 50th powerpoint.......
Deals with Important tips while using ANTIDEPRESSANTS, their special precautions, ADRs and differential mechanisms.
Will be worthwhile for a precise insight!!
Thanking all viewers who have supported me all my ways to reach this 50th milestone!!
Regards,
Vishnu. :)
complete explanation with amicable pictures regarding CNS stimulants and cognitive enhancers.useful for both UG and PG students.references from different books and authors
ANTIDEPRESSANTS: All you need to know...by RxVichu! :)RxVichuZ
This is my 50th powerpoint.......
Deals with Important tips while using ANTIDEPRESSANTS, their special precautions, ADRs and differential mechanisms.
Will be worthwhile for a precise insight!!
Thanking all viewers who have supported me all my ways to reach this 50th milestone!!
Regards,
Vishnu. :)
Major depressive disorder and its treatmentAmruta Vaidya
A concise presentation on major depressive disorder, the drug treatment options available i.e. conventional and emerging therapies which are available.
As we are getting further from the 20th century many historical facts become clearer and clearer. Looking at the past century in perspective helps us to figure out our way forward. Jung and Frankl urged humanity to assimilate the devastation of the two World Wars by taking personal responsibility, and become aware of our projections, such as nationalism. They insist that reason is not enough to prevent future tragedies. These post-World War issues were never dealt with by humanity, just swept under the rug, as in the second half of the 20th century psychiatry identified
with psychopharmacology. Moreover, psychology's self-imposed limitation to the cognitive domain alone, neglecting the study of emotion or introspection is setting the stage for the 21st century repetition of history. The idea is that the current trajectories of both psychiatry and psychology are unsustainable as they direct us towards polarization, thus opening the way for the terrible enantiodromia. The events world-wide such as geographical fragmentation and failure of the nation states are proofs that we, humans have not dealt with our dormant demons.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
1. Mechanism of Action
Classes of Antidepressant
Medications
Clinical Effects and Side Effects
2. Things I always wanted to know about
depression, but I forgot to ask
3. Response = 50% improvement of
symptoms
In the past decades the goal of treatment in
depression was a response.
Now the goal of treatment in depression is
remission and recovery.
4. Remission vs. Recovery
Remission: Patient is symptom free for 4-9
months.
Recovery: Patient is symptom free for more than 12
months.
5. STAR*D Study
In a large NIMH study called Sequenced Treatment
Alternatives to Relieve Depression(STAR*D) the goal
of treatment was remission.
Only 1/3 of patients on Citalopram monotherapy
remitted.
2/3 of patients failed to remit to Citalopram alone.
If we are talking response instead of remission – 60-
70% of patients respond to SSRI monotherapy.
6. Relapse vs. Recurrence
What is a relapse? – Getting worse during the remission phase
What is a recurrence? – Getting worse during recovery phase
7. Remission rates in MDD
Approximately one-third (33%) of depressed patients will remit during
treatment with any SSRI monotherapy.
Unfortunately, for those who fail to remit, the likelihood of remission
with another antidepressant monotherapy goes down with each
successive trial. Thus, after a year of treatment with four sequential
antidepressants (from four different classes) taken for twelve weeks
each, only two-thirds of patients will have achieved remission.
8. Common residual symptoms
In patients who do not achieve remission(but achieve response), the
most common residual symptoms are insomnia, fatigue, painful
physical complaints, problems concentrating, and lack of
interest. The least common residual symptoms are depressed mood,
suicidal ideation, and psychomotor retardation.
10. Antidepressants: complex drugs
Jules Angst(who discovered the antidepressant properties of
Imipramine) stated in 1961: “The basis for the antidepressant effect
of imipramine has not yet been elucidated, although more than
three years have passed since its introduction.” Today after 50 years
from its introduction we continue to discover new mechanisms of
action of antidepressant drugs.
These are the known mechanisms through which antidepressants exert
their actions:
1. Increase in monoamines
2. Increase in BDNF
3. Decrease in CRH
4. Increase of neurogenesis in hippocampus
5. Methylation of DNA(epigenetic factors)
6. Increase secretion of GDNF in glial cells
12. All antidepressants (except MAO inhibitors) block
monoamine transporter proteins
Serotonin Transporter(SERT)
Norepinephrine Transporter(NET)
Dopamine Transporter(DAT)
13. In the Prefrontal Cortex Blocking NET Increases both
Norepinephrine and Dopamine
In the human prefrontal cortex there are very few DAT.
As a result dopamine diffuses outside of the synapse, accumulates in
the prefrontal cortex and is eventually disposed of by NET.
Thus drugs that block NET increase both Norepinephrine and
Dopamine in the prefrontal cortex.
14.
15. What is Neurotrophin Hypothesis?
The reason why antidepressants work may not be the
fact that they increase serotonin, dopamine or
norepinephrine, but BDNF.
BDNF is produced by the neurons and is encoded by a
gene on chromosome 11.
BDNF MOLECULE encoded on CHROMOSOME 11
16. Actions of BDNF
-Sustains the viability of neurons.
-Increases dendritic arborization and
the number of synapses.
-BDNF gene is suppressed by stress
(via cortisol).
-Decreased BDNF levels lead to
neuronal atrophy and neuronal death.
- BDNF levels are low in depression,
but increase with antidepressant treatment.
- Exercise increases BDNF levels.
17. BDNF promotes formation of dendritic spines
that help the neuron respond to the environment
Axons usually form synapses with
dendrites.
In order to form a synapse the dendrite
on the receiving neuron develops tiny
hair-like growths known as spines.
In a functional synapse that is
extensively used, the spines develop
into new dendrites.
23. Serotonin Selective Reuptake
Inhibitors (SSRIs)
Six agents are in this class: Fluoxetine, Paroxetine,
Sertaline, Fluvoxamine, Citalopram and Escitalopram.
Fluvoxamine does not have an FDA indication for
depression. It was approved for social phobia and OCD. In
other countries it is being used for depression.
Three agents come in CR form: Fluoxetine, Paroxetine and
Fluvoxamine.
All are generic except Escitalopram and the CR
preparations.
24. SSRIs overview
Efficacy(FDA approved) for:
MDD (all except Fluvoxamine)
OCD( all except Citalopram and Escitalopram)
Social Phobia(Sertaline, Fluvoxamine, and Paroxetine)
PTSD(Sertaline and Paroxetine)
Bulimia(Fluoxetine)
GAD(Paroxetine and Escitalopram)
PMDD(Fluoxetine, Paroxetine CR and Sertaline)
Side Effects: GI, decreased libido, delayed ejaculation,
headaches and Insomnia/Somnolence.
25. Serotonin Norepinephrine
Reuptake Inhibitors(SNRIs)
Four agents: Venlafaxine, Desvenlafaxine, Duloxetine and
Milnacipran
Efficacy(FDA approved) for:
-Venlafaxine(MDD, GAD, Social Phobia)
-Desvenlafaxine(MDD)
-Duloxetine(MDD, GAD, neuropathic pain, fibromyalgia)
-Milnacipran(fibromyalgia)
Off label uses:
Venlafaxine (ADHD)
Duloxetine (stress urinary incontinence)
Desvenlafaxine(vasomotor symptoms associated with
menopause)
26. Norepinephrine and Dopamine
Reuptake Inhibitors(NDRIs)
One drug: Bupropion
FDA indication: MDD, smoking cessation and SAD.
Off label use: depression in cardiac patients, adjunct to
SSRIs (for depressed mood as well as to counteract sexual
side effects), substance abuse problems, ADHD and weight
loss.
Mechanism of Action: mild dopamine reuptake
inhibitor, norepinephrine reuptake inhibitor (via its
metabolite hydroxybupropion).
Adverse effects: 4/1000 risk for seizure disorder in
immediate-release formulations (doses higher than 450
mg/day) and 1/1000 in sustained release
formulations(identical to all other antidepressants).
27. Selective Norepinephrine Reuptake
Inhibitors(NRIs)
Two drugs: Atomoxetine and Reboxetine(not
approved in US).
Mechanism of Action: Block norepinephrine
transportes. In the prefrontal cortex there are very few
dopamine transporters. Norepinephrine transporters
dispose of both norepinephrine and dopamine. For
this reason when the norepinephrine transporters are
blocked the levels of both NE and DA are increased.
Atomoxetine (Strattera) has the FDA indication for
ADHD, but off label it is used as antidepressant.
28. Alpha 2 Antagonists as Serotonin and
Norepinephrine Disinhibitors(SNDIs)
One drug: Mirtazapine
FDA indication: MDD
Off label uses: panic d/o, GAD, negative symptoms of
schizophrenia, anti-nausea medication in chemotherapy
patients(Kim 2008)and post operative nausea(Chen 2008).
In STAR*D trial the combination of Mirtazapine(average
dose 36 mg/day) with Venlafaxine (average dose 210
mg/day) resulted in remission of 13% of patients who failed
three consecutive antidepressant trials(McGrath 2006).
Mechanism of action: Blocks alpha 2 adrenergic
receptors presynaptically(autoreceptors) on
noradrenergic and serotonergic neurons, leading to
disinhibition of serotonin and norepinephrine. In
addition, mirtazapine blocks 5HT2A, 5HT2C and 5HT3
postsynaptically.
29. Serotonin Antagonist/Reuptake
Inhibitors(SARIs)
Two agents: Trazodone, Nefazodone
Both have FDA indication for MDD.
Off label use:
anxiety (Trazodone),
PTSD (Nefazodone one of the most prescribed drugs for PTSD).
Depression with co-morbid substance abuse (Nefazodone).
Mechanism of Action: presynaptically blocks the serotonin
transporters and 5HT1A
postsynaptically blocks 5HT2A, 5HT2C
Adverse effects: liver damage (risk 1/250,000 per patient/year) =
If a quarter of a million patients were taking Nefazodone for a
year , one patient would be expected to develop liver damage.
30. Tricyclic Antidepressants(TCA)
Efficacy: Second or third line agents for MDD,
Panic d/o, OCD (FDA approved Clomipramine), Pain
Syndromes, Migraine prophylaxis, Enuresis (FDA approved
Imipramine).
Side Effects: dry mouth, urinary retention, constipation,
blurred vision, confusion, weight gain, sedation, sexual
dysfunction, orthostasis, tachycardia and cardiac conduction
abnormalities.
Drug interactions: TCA increase warfarin levels, cimetidine
increases TCA levels, clonidine – hypertensive crises(avoid), oral
contraceptives – increase TCA levels, SSRIs increase TCA levels,
quinidine with TCA- increase in arrhythmias(avoid), L-dopa
decreases TCA levels, sympathomimetics with TCAs – risk for
arrhythmia, HTN, tachycardia.
31. MAO Inhibitors (MAOI)
Efficacy: Third line agents for MDD, second line for
Parkinson’s disease(Selegiline).
FDA indications: treatment resistant depression.
Selegiline(Emsam) was approved by the FDA in 2006 in the transdermal
form for depression (oral Selegiline is not approved for depression).
The Selegiline dilemma: Selegiline is a MAO-B inhibitor and in the doses
used for Parkinson’s disease (5-10 mg a day) has a low risk for hypertensive
crises. Unfortunately for the treatment of depression higher doses (40-60
mg a day) are needed. At these high doses the drug affects both MAO-A
and MAO-B and the risk for hypertensive crises is high.
The transdermal Selegiline(Emsam) bypasses the gut and the liver and thus
allows for use of higher doses with lower risk for hypertensive crises(below
60 mg a day).
34. Estradiol augmentation of antidepressant
action
Estrogen has neurotrophic properties especially in the hypothalamus and
hippocampus.
During the early phase of the cycle estradiol level rises and induces dendritic
spine formation and synaptogenesis.
In the second half of the cycle (estradiol decreases and progesteron increases)
leading to removal of dendritic spines and synapses.
37. L-5-methyl-tetrahydrofolate(MTHF)
MTHF(unlike folate) crosses the BBB and activates the enzymes that
lead to the formation of NE, DA and 5HT.
These are the rate limiting enzymes such as triptophan
hydroxilase(5HT)and thyrosine hydroxilase(DA and NE).
38. Vagus Nerve Stimulation
The vagus nerve connects with the neurotransmitter centers in the
brainstem(locus coeruleus and raphe nuclei).
A pacemaker -like device is implanted in the chest wall with an implanted lead
wrapped around the vagus nerve in the neck area.
The device delivers pulses to the vagus nerve, which in turn boost monoamine
neurotransmission.
39. Transcranial Magnetic Stimulation(TMS)
Rapidly alternating current passes through a small coil placed over the scalp.
This generates a magnetic field that induces an electrical current in the DLPFC.
The affected neurons then signal other areas of the brain VMPFC and
amygdala, giving a triaminergic boost.
40. Deep Brain Stimulation
Effective for the treatment of motor complications in Parkinson’s disease and is now
used in some centers for treatment resistant depression.
Consists of a battery -powered pulse generator implanted in the chest wall like a
pacemaker.
One or two electrodes are implanted into the subgenual area of ACC .
42. Glucocorticoid Receptor Antagonists
Several reports suggested that Mifeprestone (RU-486)
was beneficial in MDD with psychotic features
(DeBattista et al. 2006)
45. Ketamine and other Glutamate Blockers
Ketamine 0.5 mg/Kg intravenously administered to patients with major
depression was found to exert a rapid (2 hours) postinfusion antidepressant
effect lasting about a week(Zarate et al. 2006).
46. "The art of medicine consists
of amusing the patient while
nature cures the disease."
Voltaire, French philosopher